THE BIPHASIC VENTILATORY RESPONSE TO HYPOXIA IN PRETERM INFANTS IS NOT DUE TO A DECREASE IN METABOLISM

The mechanism underlying the biphasic ventilatory response to hypoxia in neonates is poorly understood. Because alveolar P-CO2 (P-ACO2) decr eases and remains low during hypoxia, it has been argued that a decrea se in metabolism may occur. We hypothesized that ii the late decrease in ventilation during hypoxia is due to a decrease in CO2 production, an increase in P-ACO2 should abolish it. We studied 27 preterm infants [birth weight, 1,700 +/- 41 g (mean +/- SEM); study weight, 1,760 +/- 36 g; gestational age 32 +/- 0.2 weeks; postnatal age, 17 +/- 1 days] . A flow-through system and Beckman analyzers were used to measure Ven tilation and alveolar gases. Metabolism was expressed as changes in ox ygen consumption. Infants were studied randomly during hypoxia alone ( 15% O-2 + N-2, n = 55) and during hypoxia plus CO2 (0.5% CO2, n = 30; 2% CO2, n = 10). Each experiment consisted of 2 minutes of control mea surements (21% O-2), 5 minutes of measurements during hypoxia alone or hypoxia plus CO2, followed by 2 minutes of recovery (21% O-2). We fou nd a biphasic response to hypoxia with or without CO2 supplementation, the percent change in ventilation from initial peak hyperventilation to late hypoventilation at 5 minutes being -16 +/- 2 on 15% O-2; -9 +/ - 3 on 15% O-2 +/- 0.5% CO2; and -15 +/- 9 on 15% O-2 + 2% CO2 (P < 0. 05). The decrease in ventilation was primarily due to a significant de crease in frequency; tidal volume increased. Oxygen consumption decrea sed similarly with the various inspired gas mixtures during hypoxia. T hese findings indicate that the decrease in ventilation during hypoxia is unlikely to be solely due to a decrease in metabolism since the la te decrease in ventilation following initial hyperventilation still oc curred despite the elimination of a fall in P-ACO2. We speculate that the mechanism underlying the late decrease in Ventilation is likely of cent;al origin, probably mediated through the release of inhibitory n eurotransmitters. (C) 1996 Wiley-Liss, Inc.